Cranial cruciate ligament rupture is a leading cause of lameness in dogs, with a prevalence of 4.9% for dogs evaluated at veterinary medical teaching hospitals in North America.1 Although the epidemiological aspects are diverse, most dogs develop CrCL rupture as a result of progressive pathological ligamentous failure of unknown cause.1,2 Many theories exist, but pelvic limb conformation, in particular deformities of the proximal portion of the tibia leading to an excessive TPA, has garnered much attention as a potential cause of CrCL rupture.3–6 Tibial deformities are assessed partly through measurement of the TPA and the tibial mechanical joint orientation angles.7–11
An important aspect of CrCL rupture is that although many dogs have a history of acute lameness, they often have chronic degenerative changes that are identified on stifle joint radiographs. This suggests that the development of radiographic signs may precede the onset of clinical signs. Another important aspect of CrCL rupture is the high rate of bilateral CrCL rupture, with a lifetime prevalence of 59% to 61%.12,13 Only 4% to 17% of dogs have bilateral CrCL rupture diagnosed on initial evaluation, yet 22% to 54% of dogs with an initial diagnosis of unilateral CrCL rupture will subsequently have contralateral CrCL rupture diagnosed after a median of 10 to 17 months.12–18 As determined on the basis of Kaplan-Meier survival analysis, the median time to subsequent rupture is 947 days, with an exponential decay curve.18 This suggests that subsequent CrCL rupture is diagnosed relatively soon after the initial diagnosis in many dogs.18
The high prevalence of contralateral CrCL rupture subsequent to the initial diagnosis has profound implications for client education, the study of the etiopathogenesis, and the design of potential preventative therapeutics. Several studies12–14,16–19 have investigated potential risk factors to help identify patients at greatest risk for subsequent CrCL rupture. Two early studies14,16 highlighted the importance of bilateral stifle joint radiography in evaluating dogs with unilateral CrCL rupture. Prior to these studies,14,16 the distinction between unilateral and bilateral CrCL rupture was based solely on the clinical signs and orthopedic examination findings, and bilateral radiography was only performed if bilateral CrCL rupture was suspected on the basis of the orthopedic examination findings. In these studies,14,16 50% to 52% of dogs with unilateral CrCL rupture had radiographic findings consistent with CrCL rupture in the contralateral stifle joint. The presence and progression of these findings were both significant risk factors for subsequent contralateral CrCL rupture.14,16 These results suggest that many dogs with diagnosed unilateral CrCL rupture may actually have subclinical bilateral CrCL rupture and that the reported prevalence of bilateral CrCL rupture on initial evaluation may be highly underestimated.14,16,20
One limitation of these studies is that both inflammatory and degenerative radiographic findings of CrCL rupture were grouped together when evaluating potential risk factors for subsequent CrCL rupture.14,16,21 Radiographic effacement of the infrapatellar fat pad shadow is the primary inflammatory finding observed on stifle joint radiographs and has traditionally been termed the infrapatellar fat pad sign.22–24 The fat pad sign is one of the earliest and most consistent findings in dogs with CrCL rupture and is consistent with joint effusion, edema of the fat pad, or periarticular fibrosis.22–24 Radiographic degenerative findings (ie, the degenerative sign) include osteophytosis, enthesiophytosis, and subchondral sclerosis, which signify some degree of chronicity.22–24 Other limitations are that only 49% of the dogs in one study14 had bilateral radiography performed and that the other study16 had a small sample size. It is also unclear how many dogs were excluded from both studies14,16 because of bilateral CrCL rupture.
Other studies18,19 have since been reported, identifing lymphoplasmacytic synovitis and expression of T-lymphocyte–associated genes as significant risk factors, whereas neutering, a young age at onset, and an increased TPA of the index stifle joint have been inconsistently identified as significant risk factors for subsequent rupture.12,13,17,18 Interestingly, in these studies,12,13,17–19 bilateral radiographs were not routinely obtained and radiographic abnormalities of the contralateral stifle joint were neither assessed nor evaluated as potential risk or confounding factors for subsequent rupture. This suggests that bilateral stifle joint radiography has not yet become a standard of care when evaluating dogs with CrCL rupture.24 It also suggests that unilateral and bilateral CrCL rupture are still being distinguished on the basis of the clinical signs and orthopedic examination findings only.
The first objective of the study reported here was to retrospectively determine the prevalence of the contralateral fat pad sign and contralateral degenerative sign in a large population of dogs with unilateral CrCL rupture diagnosed on the basis of clinical signs and orthopedic examination findings and for which bilateral radiographs were available. The second objective was to independently evaluate the contralateral fat pad sign and contralateral degenerative sign as potential risk factors for subsequent rupture, controlling for potential confounding variables. The third objective was to evaluate the clinical effect of these risk factors on the pattern of subsequent CrCL rupture by use of regression model survival curves.
Materials and Methods
Case selection criteria—Medical records of dogs that underwent surgical treatment for unilateral or bilateral CrCL rupture from July 1, 2006, to June 30, 2007, were reviewed. Rupture of the CrCL was arthroscopically confirmed for all index stifle joints, and all orthopedic and arthroscopic evaluations were performed by a board-certified veterinary surgeon (KAB or IGH). On the basis of the standard of care at this hospital, preoperative bilateral orthogonal stifle joint radiographs were obtained in all cases, regardless of whether unilateral or bilateral rupture was suspected. For cases in which hip joint abnormalities were identified on orthopedic examination, preoperative lateral and ventrodorsal hip-extended pelvic radiographic views were obtained, if not already performed by the referring veterinarian. A board-certified veterinary radiologist (BJK) evaluated all radiographs prior to arthroscopic evaluation. Dogs with previous surgical treatment for CrCL rupture, concurrent or historical medial patellar luxation, pelvic limb osteochondritis dissecans, or pelvic limb trauma resulting in a fracture or additional ligamentous injuries were excluded.
On initial evaluation, unilateral and bilateral CrCL rupture were distinguished on the basis of criteria used in previous studies.12–14,16–18 Dogs with unilateral pelvic limb lameness, ipsilateral cranial tibial instability or signs of pain on full stifle joint extension, and arthroscopic confirmation of CrCL rupture were considered to have unilateral CrCL rupture. Dogs with bilateral cranial tibial instability or signs of pain on full stifle joint extension, with arthroscopic confirmation of CrCL rupture in at least 1 stifle joint, were considered to have bilateral CrCL rupture, regardless of whether bilateral pelvic limb lameness was present on gait evaluation. In addition, dogs with unilateral CrCL rupture were classified as having normal or abnormal stifle joints on the basis of contralateral stifle joint palpation. An abnormal stifle joint was defined as having palpable soft tissue swelling or medial buttress but lacking cranial tibial instability or signs of pain on stifle joint extension. Dogs with unilateral CrCL rupture were selected for risk factor analysis in this study. Dogs with bilateral CrCL rupture were included in the population proportion aspect of this study but were excluded from the risk factor analysis.
Medical records review—Information obtained from the medical record included age, sex, reproductive status, breed, body weight, body condition score, duration of lameness prior to arthroscopic evaluation, orthopedic examination findings, and preoperative radiographic and arthroscopic findings.25 For statistical comparisons, the dogs were categorized by breed as predisposed or not predisposed to CrCL rupture. The predisposed group included Newfoundlands, Rottweilers, Bulldogs, Boxers, Chow Chows, and American Staffordshire Terriers. Because of the high frequency of affected dogs, Labrador Retrievers constituted a group and all other breeds constituted a separate group. Data regarding the presence or absence of the fat pad sign and degenerative sign in both the index and contralateral stifle joints were collected from the preoperative radiology reports. Data were also collected regarding concurrent tarsal osteoarthrosis, coxofemoral dysplasia, or osteoarthrosis.
The fat pad sign was evaluated on the mediolateral radiographic view and was defined as soft tissue opacity in the cranial part of the stifle joint extending cranially to a line drawn perpendicularly from the cranial margin of the medial tibial condyle (Figure 1). This line estimates the cranial margin of the cranial poles of the menisci. Cranial extension of soft tissue opacity beyond this location was deemed excessive.
Representative mediolateral radiographic views of the stifle joints in dogs without a fat pad sign (A), with a mild fat pad sign (B), and with a marked fat pad sign (C). A—The soft tissue opacity in the cranial aspect of the stifle joint (left image) is confined caudal to a line drawn at the cranial margin of the medial tibial condyle, which is perpendicular to the tibial plateau (middle and right images). B and C—The soft tissue opacity in the cranial aspect of the stifle joint (left image) extends cranial to the line (middle and right images), causing compression of the infrapatellar fat pad. Cranial extension of the soft tissue opacity is indicated (arrows). F = Infrapatellar fat pad. P = Patellar ligament. S = Soft tissue opacity.
Citation: Journal of the American Veterinary Medical Association 244, 3; 10.2460/javma.244.3.328
Representative mediolateral radiographic views of the stifle joints in dogs without a fat pad sign (A), with a mild fat pad sign (B), and with a marked fat pad sign (C). A—The soft tissue opacity in the cranial aspect of the stifle joint (left image) is confined caudal to a line drawn at the cranial margin of the medial tibial condyle, which is perpendicular to the tibial plateau (middle and right images). B and C—The soft tissue opacity in the cranial aspect of the stifle joint (left image) extends cranial to the line (middle and right images), causing compression of the infrapatellar fat pad. Cranial extension of the soft tissue opacity is indicated (arrows). F = Infrapatellar fat pad. P = Patellar ligament. S = Soft tissue opacity.
Citation: Journal of the American Veterinary Medical Association 244, 3; 10.2460/javma.244.3.328
Representative mediolateral radiographic views of the stifle joints in dogs without a fat pad sign (A), with a mild fat pad sign (B), and with a marked fat pad sign (C). A—The soft tissue opacity in the cranial aspect of the stifle joint (left image) is confined caudal to a line drawn at the cranial margin of the medial tibial condyle, which is perpendicular to the tibial plateau (middle and right images). B and C—The soft tissue opacity in the cranial aspect of the stifle joint (left image) extends cranial to the line (middle and right images), causing compression of the infrapatellar fat pad. Cranial extension of the soft tissue opacity is indicated (arrows). F = Infrapatellar fat pad. P = Patellar ligament. S = Soft tissue opacity.
Citation: Journal of the American Veterinary Medical Association 244, 3; 10.2460/javma.244.3.328
The degenerative sign was evaluated on both the mediolateral and caudocranial radiographic views and was defined as any periarticular remodeling, osteophytes, or enthesiophyte production on the medial and lateral trochlear ridges, the distal and proximal aspects of the patella, the fabellae, the proximal and distal attachment sites of the CrCL, the proximal and distal attachment sites of the collateral ligaments, or the extensor fossa of the lateral femoral condyle. The preoperative radiographs were reviewed, and the TPA and 4 tibial mechanical joint orientation angles were measured for all dogs bilaterally; rotational or torsional deviation on the caudocranial radiographic views was assessed as described.9,10 All radiographic measurements were performed by a single author (MCF) using an image processing application.a
The surgical reports were also reviewed to determine the status of the CrCL rupture and the presence or absence of concurrent meniscal injuries. Cranial cruciate ligament rupture was classified as partial or complete on the basis of anatomic definition. Partial CrCL ruptures ranged from early fiber tearing to near complete disruption of the CrCL, with the remaining portion deemed incompetent on the basis of appearance and probing. Complete CrCL ruptures were defined as having complete disruption with no remaining intact fibers. Concurrent meniscal injuries were classified as present or absent.
Follow-up information was obtained from the medical record and from telephone calls to the primary care veterinarian. A subsequent contralateral CrCL rupture was defined as an arthroscopically confirmed rupture or detection of cranial tibial instability on stifle joint palpation for dogs whose owners declined surgical evaluation. The primary care veterinarian of dogs with long-term follow-up at their clinic was contacted and asked whether the dog developed contralateral CrCL rupture, as determined on the basis of surgical evaluation or detection of cranial tibial instability on stifle joint palpation. Dogs had follow-up until subsequent contralateral CrCL rupture, the date of their last physical examination, or the end of the data collection period (July 15, 2011).
Radiographic technique—Mediolateral radiographs were obtained with dogs in lateral recumbency with the tarsus and stifle joint at 90° flexion and the limb parallel to the digital image capture device. The x-ray beam was centered over the proximal tibial diaphysis and collimated to include the tarsus, entire tibia, and distal third of the femur. Superimposition of the femoral condyles and talar trochlea was performed to achieve correct rotational alignment. Caudocranial radiographic views were obtained with the dog in sternal recumbency and the limb extended caudally, parallel to the digital image capture device. The x-ray beam was centered over the proximal portion of the tibia and collimated similar to the mediolateral radiographic view. Correct rotational alignment was achieved by superimposing the fabellae on the femoral condyles with alignment of the medial aspect of the calcaneus to the distal intermediate ridge of the tibia.9 When there was a discrepancy for rotational alignment, preference was given to superimposing the fabellae on the femoral condyle.
Radiographic measurements—The 4 mechanical tibial joint orientation angles were measured as described.9,10 The mechanical caudoproximal tibial angle and mechanical craniodistal tibial angle were measured from the mediolateral tibial radiographs, and the mechanical medioproximal tibial angle and mechanical mediodistal tibial angle were measured from the caudocranial tibial radiographs. The sagittal plane mechanical axis was drawn from the central aspect of the talus, extending proximally to bisect the midpoint between the apices of the medial and lateral intercondylar eminences.10 The proximal tibial joint orientation line was drawn from the cranial and caudal aspects of the medial tibial condyle, and the distal tibial joint orientation line was drawn along the distal aspect of the distal intermediate ridge of the tibia cranially and the caudodistal aspect of the cochlea tibiae caudally.10 The mechanical caudoproximal tibial angle and mechanical craniodistal tibial angle were formed at the intersection of the mechanical axis and joint orientation lines along the caudoproximal and craniodistal aspects of the tibia, respectively.10 The TPA was calculated as the complement of the mechanical caudoproximal tibial angle (TPA = 90° – mechanical caudoproximal tibial angle).10 The frontal plane mechanical axis was drawn from the most distal aspect of the distal intermediate ridge of the tibia, extending proximally to the proximal central aspect of the femoral intercondylar fossa. Joint orientation lines were drawn along the most distal aspects of the medial and lateral tibial condyles for the proximal portion of the tibia and along the most proximal aspects of the medial and lateral arciform grooves of the cochlea tibiae for the distal portion of the tibia.9 The mechanical medioproximal tibial angle and mechanical mediodistal tibial angle were formed at the intersection of the mechanical axis and joint orientation lines along the proximomedial and distomedial aspects of the tibia, respectively.9
Assessment for rotational or torsional deviation was performed on the caudocranial tibial radiographic views.9 The transverse distance from the center of the distal intermediate ridge of the tibia to the medial aspect of the tuber calcaneus was measured and divided by the distance between the most proximal aspects of the medial and lateral arciform grooves of the cochlea tibiae.9 This value was expressed as the percentage deviation.9 Positive integers were used to indicate lateral deviation, and negative integers were used to indicate medial deviation of the calcaneus with respect to the distal aspect of the intermediate ridge of the tibia.
Statistical analysis—The associations of potential predictive variables with the rates of subsequent contralateral CrCL rupture were evaluated with Cox proportional hazards regression models separately for all dogs with unilateral CrCL rupture (n = 96) and for dogs with unilateral CrCL rupture in the normal contralateral stifle joint group (84). For both groups, univariate models were initially fit, and variables with values of P < 0.05 (corresponding to a test of the null hypothesis that the regression coefficient = 0) were included in multivariate models that contained at least 1 variable with a value of P < 0.05. On the basis of the results of previous studies, age, body weight, duration of lameness, breed, index TPA, and contralateral TPA were included as confounding variables in all multivariate models. Additional variables were included if they changed the hazard ratio estimate by ≥ 10%. Proportionality was verified by examining the interaction between variables and the natural log of time. Results are presented as hazard ratios with 95% CIs. Regression models were also used to generate survival curves and estimate the median time to and the 3-year probability of subsequent contralateral CrCL rupture. All statistical analyses were performed with a commercially available software program.b
Results
One hundred eighty-two dogs underwent stifle joint arthroscopy for CrCL rupture during the study period. Sixty-four dogs were excluded because of previous surgical treatment for CrCL rupture, concurrent or historical medial patellar luxation, pelvic limb osteochondritis dissecans, or pelvic limb trauma resulting in a fracture or additional ligamentous injuries. No dogs had CrCL avulsion fractures. All remaining dogs (n = 118) had complete medical records and bilateral radiographs available. Among these dogs, 96 (81.4%) had unilateral CrCL rupture and 22 (18.6%) had bilateral CrCL rupture. Of the dogs with unilateral CrCL rupture, 84 (87.5%) were classified as having a normal contralateral stifle joint and 12 (12.5%) were classified as having an abnormal contralateral stifle joint, as determined on palpation of the contralateral stifle joint.
Prevalence of the fat pad sign and degenerative sign—A fat pad sign was present in the index stifle joint for all dogs with unilateral CrCL rupture with normal contralateral stifle joints and bilaterally for all dogs with unilateral CrCL rupture with abnormal contralateral stifle joints as well as those with bilateral CrCL rupture. A fat pad sign was present in the contralateral stifle joint for 41 of the 96 (42.7%) dogs with unilateral CrCL rupture and 29 of the 84 (34.5%) dogs with unilateral CrCL rupture and normal contralateral stifle joints (ie, dogs with unilateral CrCL rupture excluding dogs with abnormal contralateral stifle joints). Among all 118 dogs evaluated in this study, 63 (53.4%) had a fat pad sign bilaterally.
A degenerative sign was present in the index stifle joint for 89 of the 96 (92.7%) dogs with unilateral CrCL rupture and 77 of the 84 (91.7%) dogs with unilateral CrCL rupture with normal contralateral stifle joints. A degenerative sign was present bilaterally for all dogs with unilateral CrCL rupture with abnormal contralateral stifle joints and 21 of 22 (95.5%) with bilateral CrCL rupture. A degenerative sign was present in the contralateral stifle joint for 43 of the 96 (44.8%) dogs with unilateral CrCL rupture and 31 of the 84 (36.9%) dogs with unilateral CrCL rupture with normal contralateral stifle joints. Among all 118 dogs evaluated in this study, 65 (55.1%) had a degenerative sign bilaterally.
Of the 96 dogs with unilateral CrCL rupture, 49 (51.0%) had either a contralateral fat pad sign or a contralateral degenerative sign and 35 (36.5%) had both. Of the 84 dogs with unilateral CrCL rupture and normal contralateral stifle joints, 37 (44.0%) had either a contralateral fat pad sign or a contralateral degenerative sign and 23 (27.4%) had both.
Potential confounding variables—Among the 96 dogs with unilateral CrCL rupture, 30 (31.3%) were Labrador Retrievers, 14 (14.5%) were from predisposed breeds, and 52 (54.2%) were from other breeds. Thirty-five breeds were represented. There were 59 (61.5%) spayed females, 3 (3.1%) sexually intact females, 28 (29.2%) neutered males, and 6 (6.3%) sexually intact males. Mean ± SD age at the time of initial diagnosis was 5.5 ± 2.5 years (median, 5.5 years; range, 0.9 to 11.3 years). Mean ± SD body weight was 34.5 ± 13.2 kg (76.0 ± 29.0 lb; median, 33.2 kg [73.0 lb]; range, 2.7 to 85.0 kg [5.9 to 187.0 lb]), with a mean ± SD body condition score of 6.1 ± 1.0 (median, 6/9; range, 4/9 to 9/9). The mean ± SD duration of lameness was 90.6 ± 100.4 days (median, 60 days; range, 3 to 730 days). Of the 96 dogs with unilateral CrCL rupture, 14 (14.5%) had radiographic evidence of hip joint dysplasia or osteoarthrosis and 5 (5.2%) had radiographic tarsal osteoarthrosis. On arthroscopic evaluation of the index stifle joints (n = 96), 46 (47.9%) had medial meniscal injuries, 58 (60.4%) had a complete CrCL rupture, and 36 (37.5%) had both. The mean ± SD TPA was 27.4 ± 4.4° (median, 27°; range, 16° to 42°) for the index limb and 26.7 ± 4.0° (median, 27°; range, 16° to 39°) for the contralateral limb.
Of the 84 dogs with unilateral CrCL rupture with normal contralateral stifle joints, 28 (33.3%) were Labrador Retrievers, 11 (13.1%) were from predisposed breeds, and 45 (53.6%) were from other breeds. There were 51 (60.7%) spayed females, 2 (2.4%) sexually intact females, 26 (31.0%) neutered males, and 5 (6.0%) sexually intact males. The mean ± SD age at the time of initial diagnosis was 5.6 ± 2.6 years (median, 5.8 years; range, 0.9 to 11.3 years). The mean ± SD body weight was 33.2 ± 11.6 kg (73.0 ± 25.5 lb; median, 33.1 kg [72.8 lb]; range, 2.7 to 80.1 kg [5.9 to 176.2 lb]), with a mean ± SD body condition score of 6.0 ± 1.0 (median, 6/9; range, 4/9 to 8/9). The mean ± SD duration of lameness was 86.8 ± 101.8 days (median, 60 days; range, 3 to 730 days). Of the 84 dogs with unilateral CrCL rupture with normal contralateral stifle joints, 14 (16.7%) had radiographic evidence of hip joint dysplasia or osteoarthrosis and 4 (4.8%) had radiographic tarsal osteoarthrosis. On arthroscopic evaluation of the index stifle joint (n = 84), 39 (46.4%) had medial meniscal injuries, 54 (64.3%) had a complete CrCL rupture, and 34 (40.5%) had both. The mean ± SD TPA was 27.4 ± 4.6° (median, 27°; range, 16° to 42°) for the index limb and 26.8 ± 4.1° (median, 27°; range, 16° to 39°) for the contralateral limb.
The mean ± SD and frequency of potential confounding variables for all of the dogs with unilateral CrCL rupture and for those with normal contralateral stifle joints, with respect to the contralateral fat pad sign and contralateral degenerative sign, as well as for the dogs with unilateral CrCL rupture with abnormal contralateral stifle joints and those with bilateral CrCL rupture are summarized (Tables 1 and 2).
Mean ± SD values and frequency (No. [%]) of potential confounding variables with respect to the contralateral fat pad sign in dogs with CrCL rupture.
| Contralateral fat pad sign | |||||
|---|---|---|---|---|---|
| Absent | Present | ||||
| Unilateral CrCl rupture | |||||
| Variable | Unilateral CrCl rupture and normal contralateral stifle joint (n = 55) | Total (n = 41) | Normal contralateral stifle joint (n = 29) | Abnormal contralateral stifle joint (n = 12) | Bilateral CrCl rupture (n = 22) |
| Age (y) | 6.0 ± 2.5 | 4.9 ± 2.4 | 5.0 ± 2.5 | 4.4 ± 1.8 | 5.6 ± 2.8 |
| Weight (kg) | 32.0 ± 10.5 | 38.0 ± 15.7 | 35.6 ± 13.5 | 43.6 ± 19.7 | 35.1 ± 9.0 |
| Body condition score (scale of 1–9) | 5.9 ± 1.0 | 6.3 ± 1.0 | 6.2 ± 1.0 | 6.4 ± 0.9 | 5.9 ± 0.9 |
| Lameness duration (d) | 86.1 ± 83.2 | 96.6 ± 120.6 | 88.1 ± 131.9 | 117.1 ± 89.2 | 171.6 ± 195.3 |
| Sex | |||||
| Sexually intact male | 4 (7.3) | 2 (4.9) | 1 (3.4) | 1 (8.3) | 2 (9.1) |
| Neutered male | 16 (29.1) | 12 (29.3) | 10 (34.5) | 2 (16.7) | 5 (22.7) |
| Sexually intact female | 1 (1.8) | 2 (4.9) | 1 (3.4) | 1 (8.3) | 1 (4.5) |
| Spayed female | 34 (61.8) | 25 (61.0) | 17 (58.6) | 8 (66.7) | 14 (63.6) |
| Breed | |||||
| Labrador Retriever | 18 (32.7) | 12 (29.3) | 10 (34.5) | 2 (16.7) | 8 (36.4) |
| Predisposed | 6 (10.9) | 8 (19.5) | 5 (17.2) | 3 (25.0) | 6 (27.3) |
| Other | 31 (56.4) | 21 (51.2) | 14 (48.3) | 7 (58.3) | 8 (36.4) |
| CrCL rupture | |||||
| Partial | 21 (38.2) | 17 (41.5) | 9 (31.0) | 8 (66.7) | 8 (36.4) |
| Complete | 34 (61.8) | 24 (58.5) | 20 (69.0) | 4 (33.3) | 14 (63.6) |
| Meniscus | |||||
| Intact | 28 (50.9) | 22 (53.7) | 17 (58.6) | 5 (41.7) | 14 (63.6) |
| Torn | 27 (49.1) | 19 (46.3) | 12 (41.4) | 7 (58.3) | 8 (36.4) |
| Hip joint disease | |||||
| No | 45 (81.8) | 37 (90.2) | 25 (86.2) | 12 (100.0) | 19 (86.4) |
| Yes | 10 (18.2) | 4 (9.8) | 4 (13.8) | 0 (0.0) | 3 (13.6) |
| Tarsal joint disease | |||||
| No | 51 (92.7) | 40 (97.6) | 29 (100.0) | 11 (91.7) | 18 (81.8) |
| Yes | 4 (7.3) | 1 (2.4) | 0 (0.0) | 1 (8.3) | 4 (18.2) |
| TPA (°) | |||||
| Index joint | 27.7 ± 4.5 | 26.8 ± 4.2 | 26.7 ± 4.7 | 27.2 ± 2.9 | 25.8 ± 2.9 |
| Contralateral joint | 27.1 ± 3.6 | 26.2 ± 4.4 | 26.1 ± 4.8 | 26.4 ± 3.3 | 24.9 ± 3.8 |
| mCaPTA (°) | |||||
| Index joint | 62.3 ± 4.5 | 63.2 ± 4.2 | 63.3 ± 4.7 | 62.8 ± 2.9 | 64.2 ± 2.9 |
| Contralateral joint | 62.9 ± 3.6 | 63.8 ± 4.4 | 63.9 ± 4.8 | 63.6 ± 3.3 | 65.1 ± 3.8 |
| mCrDTA (°) | |||||
| Index joint | 80.8 ± 4.7 | 80.4 ± 2.8 | 80.6 ± 3.1 | 80.1 ± 2.3 | 81.6 ± 3.9 |
| Contralateral joint | 80.3 ± 5.1 | 80.3 ± 3.2 | 80.8 ± 3.4 | 79.3 ± 2.1 | 81.2 ± 3.4 |
| mMPTA (°) | |||||
| Index joint | 93.8 ± 2.9 | 92.7 ± 2.3 | 92.9 ± 2.4 | 92.1 ± 2.2 | 93.2 ± 2.0 |
| Contralateral joint | 93.2 ± 2.6 | 92.6 ± 2.9 | 92.8 ± 3.2 | 92.2 ± 2.2 | 93.4 ± 2.0 |
| mMDTA (°) | |||||
| Index joint | 95.3 ± 3.1 | 95.8 ± 2.4 | 95.4 ± 2.1 | 96.7 ± 3.0 | 96.2 ± 2.8 |
| Contralateral joint | 95.0 ± 3.0 | 95.5 ± 2.0 | 95.4 ± 2.1 | 95.9 ±1.7 | 96.0 ± 2.0 |
| Deviation (%) | |||||
| Index joint | 7.7 ± 16.7 | 17.4 ± 16.6 | 13.2 ± 15.1 | 27.4 ± 16.5 | 10.2 ± 12.7 |
| Contralateral joint | 3.9 ± 16.7 | 17.9 ± 13.2 | 15.9 ± 11.1 | 22.8 ± 16.8 | 12.2 ± 13.9 |
Predisposed = Newfoundland, Rottweiler, Bulldog, Boxer, Chow Chow, and American Staffordshire Terrier. mCaPTA = Mechanical caudoproximal tibial angle. mCrDTA = Mechanical craniodistal tibial angle. mMDTA = Mechanical mediodistal tibial angle. mMPTA = Mechanical medioproximal tibial angle.
Mean ± SD values and frequency (No. [%]) of potential confounding variables with respect to the contralateral degenerative sign in dogs with CrCL rupture.
| Degenerative sign | |||||
|---|---|---|---|---|---|
| Absent | Present | ||||
| Unilateral CrCl rupture | |||||
| Variable | Unilateral CrCl rupture and normal contralateral stifle joint (n = 53) | Total (n = 43) | Normal contralateral stifle joint (n = 31) | Abnormal contralateral stifle joint (n = 12) | Bilateral CrCl rupture (n = 22) |
| Age (y) | 5.9 ± 2.6 | 5.0 ± 2.3 | 5.3 ± 2.5 | 4.4 ± 1.8 | 5.6 ± 2.8 |
| Weight (kg) | 33.1 ± 11.8 | 36.3 ± 14.7 | 33.5 ± 11.5 | 43.6 ± 19.7 | 35.1 ± 9.0 |
| Body condition score (scale of 1– 9) | 6.0 ± 1.0 | 6.1 ± 1.0 | 6.1 ± 1.1 | 6.4 ± 0.9 | 5.9 ± 0.9 |
| Lameness duration (d) | 79.2 ± 80.0 | 104.5 ± 120.5 | 99.7 ± 131.6 | 117.1 ± 89.2 | 171.6 ± 195.3 |
| Sex | |||||
| Sexually intact male | 5 (9.4) | 1 (2.3) | 0 (0.0) | 1 (8.3) | 2 (9.1) |
| Neutered male | 16 (30.2) | 12 (27.9) | 10 (32.3) | 2 (16.7) | 5 (22.7) |
| Sexually intact female | 1 (1.9) | 2 (4.7) | 1 (3.2) | 1 (8.3) | 1 (4.5) |
| Spayed female | 31 (58.5) | 28 (65.1) | 20 (64.5) | 8 (66.7) | 14 (63.6) |
| Breed | |||||
| Labrador Retriever | 18 (34.0) | 12 (27.9) | 10 (32.3) | 2 (16.7) | 8 (36.4) |
| Predisposed | 6 (11.3) | 8 (18.6) | 5 (16.1) | 3 (25.0) | 6 (27.3) |
| Other | 29 (54.7) | 23 (53.5) | 16 (51.6) | 7 (58.3) | 8 (36.4) |
| CrCL rupture | |||||
| Partial | 19 (35.8) | 19 (44.2) | 11 (35.5) | 8 (66.7) | 8 (36.4) |
| Complete | 34 (64.2) | 24 (55.8) | 20 (64.5) | 4 (33.3) | 14 (63.6) |
| Meniscus | |||||
| Intact | 26 (49.1) | 24 (55.8) | 19 (61.3) | 5 (41.7) | 14 (63.6) |
| Torn | 27 (50.9) | 19 (44.2) | 12 (38.7) | 7 (58.3) | 8 (36.4) |
| Hip joint disease | |||||
| No | 44 (83.0) | 38 (88.4) | 26 (83.9) | 12 (100.0) | 19 (86.4) |
| Yes | 9 (17.0) | 5 (11.6) | 5 (16.1) | 0 (0.0) | 3 (13.6) |
| Tarsal joint disease | |||||
| No | 49 (92.5) | 42 (97.7) | 31 (100.0) | 11 (91.7) | 18 (81.8) |
| Yes | 4 (7.5) | 1 (2.3) | 0 (0.0) | 1 (8.3) | 4 (18.2) |
| TPA (°) | |||||
| Index joint | 27.4 ± 4.5 | 27.3 ± 4.3 | 27.4 ± 4.8 | 27.2 ± 2.9 | 25.8 ± 2.9 |
| Contralateral joint | 26.7 ± 3.7 | 26.8 ± 4.3 | 26.9 ± 4.7 | 26.4 ± 3.3 | 24.9 ± 3.8 |
| mCaPTA (°) | |||||
| Index joint | 62.6 ± 4.5 | 62.7 ± 4.3 | 62.6 ± 4.8 | 62.8 ± 2.9 | 64.2 ± 2.9 |
| Contralateral joint | 63.3 ± 3.7 | 63.2 ± 4.3 | 63.1 ± 4.7 | 63.6 ± 3.3 | 65.1 ± 3.8 |
| mCrDTA (°) | |||||
| Index joint | 81.0 ± 4.0 | 80.3 ± 4.0 | 80.3 ± 4.5 | 80.1 ± 2.3 | 81.6 ± 3.9 |
| Contralateral joint | 80.3 ± 4.6 | 80.5 ± 4.2 | 80.9 ± 4.7 | 79.3 ± 2.1 | 81.2 ± 3.4 |
| mMPTA (°) | |||||
| Index joint | 93.6 ± 3.0 | 92.9 ± 2.3 | 93.3 ± 2.3 | 92.1 ± 2.2 | 93.2 ± 2.0 |
| Contralateral joint | 93.0 ± 2.9 | 92.9 ± 2.5 | 93.2 ± 2.6 | 92.2 ± 2.2 | 93.4 ± 2.0 |
| mMDTA (°) | |||||
| Index joint | 95.3 ± 3.0 | 95.8 ± 2.6 | 95.4 ± 2.4 | 96.7 ± 3.0 | 96.2 ± 2.8 |
| Contralateral joint | 95.1 ± 3.0 | 95.4 ± 2.5 | 95.2 ± 2.3 | 95.9 ± 1.7 | 96.0 ± 2.0 |
| Deviation (%) | |||||
| Index joint | 9.0 ± 17.1 | 15.3 ± 17.1 | 10.6 ± 15.1 | 27.4 ± 16.5 | 10.2 ± 12.7 |
| Contralateral joint | 4.2 ± 17.4 | 16.9 ± 12.8 | 14.6 ± 10.4 | 22.8 ± 16.8 | 12.2 ± 13.9 |
See Table 1 for key.
Univariate and multivariate analyses—The contralateral fat pad sign and contralateral degenerative sign were significant risk factors for subsequent contralateral CrCL rupture for the dogs with unilateral CrCL rupture and the subgroup with normal contralateral stifle joints (Table 3). The presence of palpable abnormalities of the contralateral stifle joint was also a significant risk factor for subsequent CrCL rupture for dogs with unilateral CrCL rupture. All potential confounding variables (age, body weight, body condition score, sex, reproductive status, breed, duration of lameness, presence of meniscal injury, partial or complete CrCL rupture, concurrent hip joint dysplasia or osteoarthrosis, concurrent tarsal osteoarthrosis, index and contralateral TPA, tibial mechanical joint orientation angles, and percentage deviation) lacked significance on univariate analysis for the dogs with unilateral CrCL rupture and the subgroup with normal contralateral stifle joints.
Univariate and multivariate results for all dogs with unilateral CrCL rupture and those with normal contralateral stifle joints with respect to the contralateral fat pad sign, contralateral degenerative sign, and contralateral stifle joint palpation.
| Univariate | Multivariate | |||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Variable | Hazard ratio | 95% CI | P value | Median time to subsequent rupture (d) | 1-year probability (%) | 2-year probability (%) | 3-year probability (%) | Hazard ratio | 95% CI | P value | Median time to subsequent rupture (d) | 1-year probability (%) | 2-year probability (%) | 3-year probability (%) |
| Contralateral fat pad sign* | Unilateral CrCL rupture | |||||||||||||
| Absent (n = 55) | 1 | — | — | 1,685 | 14.0 | 27.0 | 29.4 | 1 | — | — | 1,693 | 10.7 | 22.6 | 25.1 |
| Present (n = 41) | 5.0 | 2.8–8.9 | < 0.001 | 348 | 53.3 | 79.5 | 82.7 | 7.0 | 3.7–13.4 | < 0.001 | 274 | 54.5 | 83.4 | 86.8 |
| Overall (n = 96) | — | — | — | 970 | 26.1 | 46.7 | 50.1 | — | — | — | 1,156 | 22.8 | 44.5 | 48.5 |
| Unilateral CrCL rupture and normal contralateral stifle joints | ||||||||||||||
| Absent (n = 55) | 1 | — | — | 1,683 | 11.5 | 26.7 | 29.5 | 1 | — | — | 1,688 | 8.5 | 22.0 | 24.9 |
| Present (n = 29) | 4.8 | 2.6–8.9 | < 0.001 | 425 | 44.4 | 77.4 | 81.4 | 6.7 | 3.3–13.6 | < 0.001 | 421 | 44.7 | 80.9 | 85.3 |
| Overall (n = 84) | — | — | — | 1,304 | 19.0 | 41.3 | 45.2 | — | — | — | 1,321 | 15.7 | 38.0 | 42.4 |
| Contralateral degenerative sign† | ||||||||||||||
| Unilateral CrCL rupture | ||||||||||||||
| Absent (n = 53) | 1 | — | — | 1,380 | 19.8 | 34.8 | 37.4 | 1 | — | — | 1,358 | 18.5 | 35.8 | 38.9 |
| Present (n = 43) | 2.5 | 1.5–4.4 | < 0.001 | 472 | 43.1 | 66.4 | 69.7 | 2.2 | 1.2–4.1 | 0.013 | 550 | 36.0 | 62.1 | 66.0 |
| Overall (n = 96) | — | — | — | 965 | 28.5 | 47.8 | 50.9 | — | — | — | 968 | 25.2 | 46.7 | 50.4 |
| Unilateral CrCL rupture and normal contralateral stifle joints | ||||||||||||||
| Absent (n = 53) | 1 | — | — | 1,376 | 16.7 | 34.7 | 37.8 | 1 | — | — | 1,669 | 14.4 | 31.1 | 34.3 |
| Present (n = 31) | 2.1 | 1.2–3.8 | 0.016 | 560 | 32.0 | 59.2 | 63.2 | 2.3 | 1.2–4.4 | 0.008 | 582 | 30.4 | 58.2 | 62.6 |
| Overall (n = 84) | — | — | — | 1,295 | 21.4 | 43.0 | 46.5 | — | — | — | 1,320 | 19.1 | 40.0 | 43.7 |
| Contralateral stifle palpation‡ | ||||||||||||||
| Unilateral CrCL rupture | ||||||||||||||
| Normal (n = 84) | 1 | — | — | 1,304 | 25.5 | 43.5 | 46.4 | 1 | — | — | 1,688 | 20.8 | 39.6 | 43.0 |
| Abnormal (n = 12) | 3.9 | 1.9–7.9 | < 0.001 | 223 | 68.3 | 89.2 | 91.2 | 5.8 | 2.2–15.5 | < 0.001 | 188 | 74.3 | 94.7 | 96.2 |
| Overall (n = 96) | — | — | — | 764 | 29.5 | 49.2 | 52.2 | — | — | — | 968 | 25.2 | 46.7 | 50.4 |
Addition of the index mechanical medioproximal tibial angle as a confounding variable.
Addition of contralateral stifle joint palpation as a confounding variable.
Addition of contralateral degenerative sign as a confounding variable.
Age, body weight, duration of lameness, breed, index TPA, and contralateral TPA were included in all multivariate models as confounding factors.
Contralateral CrCL outcome—Subsequent contralateral CrCL rupture was diagnosed in 54 of the 96 (56.3%) dogs with unilateral CrCL rupture, 44 of the 84 (52.4%) dogs with unilateral CrCL rupture with normal contralateral stifle joints, and 10 of the 12 dogs with unilateral CrCL rupture with abnormal contralateral stifle joints. Contralateral CrCL rupture concurrent or subsequent to the diagnosis occurred in 76 of 118 (64.4%) dogs. Cox regression–derived probability curves of the time to subsequent contralateral CrCL rupture were plotted for all dogs with unilateral CrCL rupture and those with normal contralateral stifle joints with respect to the contralateral fat pad sign and contralateral degenerative sign (Figure 2). The median time to subsequent rupture and 3-year probability of subsequent rupture for all dogs with unilateral CrCL rupture and those with normal contralateral stifle joints with respect to the contralateral fat pad sign, contralateral degenerative sign, and contralateral stifle joint palpation were summarized (Table 3).
Cox regression-derived probability curves of the time to subsequent contralateral CrCL rupture for 96 dogs with unilateral CrCL rupture (A and B) and 84 of those dogs that had normal (Normal) contralateral stifle joints (C and D) as determined by contralateral stifle joint palpation with respect to the presence (dashed line) or absence (solid line) of the contralateral fat pad sign and contralateral degenerative sign. UR = Unilateral rupture. w/o = Without.
Citation: Journal of the American Veterinary Medical Association 244, 3; 10.2460/javma.244.3.328
Cox regression-derived probability curves of the time to subsequent contralateral CrCL rupture for 96 dogs with unilateral CrCL rupture (A and B) and 84 of those dogs that had normal (Normal) contralateral stifle joints (C and D) as determined by contralateral stifle joint palpation with respect to the presence (dashed line) or absence (solid line) of the contralateral fat pad sign and contralateral degenerative sign. UR = Unilateral rupture. w/o = Without.
Citation: Journal of the American Veterinary Medical Association 244, 3; 10.2460/javma.244.3.328
Cox regression-derived probability curves of the time to subsequent contralateral CrCL rupture for 96 dogs with unilateral CrCL rupture (A and B) and 84 of those dogs that had normal (Normal) contralateral stifle joints (C and D) as determined by contralateral stifle joint palpation with respect to the presence (dashed line) or absence (solid line) of the contralateral fat pad sign and contralateral degenerative sign. UR = Unilateral rupture. w/o = Without.
Citation: Journal of the American Veterinary Medical Association 244, 3; 10.2460/javma.244.3.328
The median follow-up times for dogs with subsequent rupture were 418 days (range, 35 to 1,715 days) for dogs with unilateral CrCL rupture, 503 days (range, 49 to 1,715 days) for dogs with unilateral CrCL rupture with normal contralateral stifle joints, and 153 days (range, 35 to 1,309 days) for dogs with unilateral CrCL rupture with abnormal contralateral stifle joints. The median follow-up times for dogs without subsequent rupture were 1,311 days (range, 20 to 1,816 days) for all dogs with unilateral CrCL rupture and 1,311 days (range, 20 to 1,816 days) for dogs with unilateral CrCL rupture with normal contralateral stifle joints. The follow-up times for the 2 dogs with unilateral CrCL rupture with abnormal contralateral stifle joints that did not develop subsequent contralateral rupture were 28 and 1,493 days. Subsequent contralateral CrCL ruptures were confirmed surgically in 45 of the 54 (83.3%) dogs with unilateral CrCL rupture, 36 of the 44 (81.8%) dogs with unilateral CrCL rupture with normal contralateral stifle joints, and 9 of the 10 dogs with unilateral CrCL rupture with abnormal contralateral stifle joints. The remaining subsequent contralateral CrCL ruptures were diagnosed on the basis of the presence of cranial tibial instability on palpation because the owners declined further surgical intervention. For dogs without subsequent rupture, 11 of the 42 (26.2%) dogs with unilateral CrCL rupture, 10 of the 40 (25%) dogs with unilateral CrCL rupture with normal contralateral stifle joints, and 1 of 2 of the dogs with unilateral CrCL rupture with abnormal contralateral stifle joints were evaluated by a board-certified surgeon (KAB or IGH). Primary care veterinarians evaluated the remaining dogs.
Discussion
The contralateral fat pad sign and contralateral degenerative sign were prevalent in dogs with unilateral CrCL rupture and were significant risk factors for subsequent contralateral CrCL rupture. Findings on contralateral stifle joint palpation were also identified as significant predictors for subsequent contralateral CrCL rupture in dogs with unilateral CrCL rupture. On the basis of palpable and radiographic abnormalities consistent with CrCL rupture in the contralateral stifle joint and the association with greatly reduced time to subsequent rupture, we strongly suspect that the dogs with unilateral CrCL rupture with abnormal contralateral stifle joints had subclinical bilateral CrCL rupture. In an effort to be consistent with the published literature and to make our results comparable, we included dogs with unilateral CrCL rupture and abnormal contralateral stifle joints in the unilateral CrCL rupture group.12–14,18,20 This also allowed for separate analyses for all dogs with unilateral CrCL rupture and for only those with normal contralateral stifle joints. Compared with published data,12,13,18 the percentage of dogs with bilateral CrCL rupture diagnosed on initial evaluation was remarkably similar, as was the median time to subsequent contralateral CrCL rupture for the dogs with unilateral CrCL rupture. Although unclear in prior studies,12–14,18,20 given these similarities, we suspect that dogs with unilateral CrCL rupture with characteristics of abnormal contralateral stifle joints in other studies might also have been classified as having unilateral CrCL rupture. If the dogs with unilateral CrCL rupture with abnormal contralateral stifle joints in this study had been classified as having bilateral CrCL rupture, the percentage of dogs with bilateral CrCL rupture (28.8%) would have been unprecedented.
The purpose of analyzing the dogs with unilateral CrCL rupture with normal contralateral stifle joints separately was to remove potential bias as a result of misclassifying some dogs with bilateral CrCL rupture (dogs with unilateral CrCL rupture with abnormal contralateral stifle joints) as having unilateral CrCL rupture. This analysis confirmed that the contralateral fat pad sign and contralateral degenerative sign were prevalent in dogs with unilateral CrCL rupture diagnosed on the basis of orthopedic examination findings. Although the contralateral fat pad sign and contralateral degenerative sign were both significant risk factors for subsequent contralateral CrCL rupture, the contralateral fat pad sign had the higher hazard ratio and greater association with the time to subsequent rupture. Clinically, the fat pad sign and degenerative sign are closely linked. The fat pad sign is invariably present in all cases of CrCL rupture, and the degenerative sign is often present and is related to the chronicity and severity of the CrCL rupture.22–24
The high prevalence and association with greatly reduced time to subsequent rupture suggest that many dogs with unilateral CrCL rupture and a positive contralateral fat pad sign have subclinical bilateral CrCL rupture. This suggestion is exemplified in a recent study20 of 16 dogs with CrCL rupture and a positive contralateral fat pad sign. Despite the fact that all 16 dogs had unilateral CrCL rupture diagnosed on the basis of the orthopedic examination and stress radiography, arthroscopic evaluation revealed that 12 dogs had partial rupture of the contralateral CrCL.20 Although it was unclear whether these dogs determined to have unilateral CrCL rupture would be classified as having palpably normal or abnormal contralateral stifle joints, these results support the notion that a high percentage of dogs with a positive contralateral fat pad sign have subclinical bilateral CrCL rupture. In contrast to these results, another author with extensive clinical observational experience suggested that the correlation of a positive contralateral fat pad sign with contralateral CrCL rupture is even higher (approx 99%).26
The major limitation of the present study was the lack of bilateral stifle joint arthroscopy. Had bilateral arthroscopy been performed, the true prevalence of bilateral CrCL rupture at the time of initial evaluation could have been determined. Arthroscopic evaluation of the contralateral stifle joint would also clarify the importance of the contralateral fat pad sign, with respect to the status of the contralateral CrCL. Because of this limitation, the results of this study can only support an association of the contralateral fat pad sign and contralateral degenerative sign with a shorter time to subsequent contralateral CrCL rupture. Clearly, a prospective study involving bilateral arthroscopy in a large number of dogs with previously diagnosed unilateral CrCL rupture and a positive contralateral fat pad sign is needed.
Despite this limitation, the results of this study support the practice of obtaining bilateral stifle joint radiographs for all dogs with CrCL rupture. Regardless of whether a positive contralateral fat pad sign or degenerative sign represents subclinical bilateral CrCL rupture, they are clearly major risk factors for the development of clinical signs associated with contralateral CrCL rupture. This information is valuable for client education. With such a high prevalence of subsequent contralateral CrCL rupture, the results of this study also support the practice of performing bilateral stifle joint arthroscopy for any dog with a positive contralateral fat pad sign. If a contralateral CrCL rupture is diagnosed, earlier surgical intervention may improve treatment outcomes. This is supported by the results of another study,27 in which earlier surgical intervention was suspected to provide protection against further CrCL disruption and secondary meniscal and articular cartilage pathological changes.
Given their high prevalence and association with reduced time to subsequent rupture, the contralateral fat pad sign and degenerative sign should be considered in future studies investigating potential disease-modifying treatments. In a previous study,18 16 dogs with unilateral CrCL rupture and a positive contralateral fat pad sign underwent evaluation of a potential disease-modifying treatment for contralateral CrCL rupture. Following bilateral stifle joint arthroscopy and surgical treatment of the index stifle joint, the contralateral stifle joint was injected with hyaluronic acid, followed by a 10-week course of oral administration of doxycycline.18 Those investigators concluded that this regimen of disease-modifying treatment had no effect on the rate of subsequent rupture; however, their comparisons were made against an overall median time to subsequent rupture of 947 days for all dogs with unilateral CrCL rupture.18 The 16 dogs in the present study would be classified as having unilateral CrCL rupture with a positive contralateral fat pad sign, with a potentially reduced pretreatment median time to subsequent rupture. If they had compared the outcome to the median time to subsequent rupture for dogs with unilateral CrCL rupture with a positive fat pad sign, a clinically relevant improvement may have been found.
Although it has not been clinically evaluated, the definition of the fat pad sign used in this study was similar to the definition listed in a current surgery reference.24 The intention of the present study was not to standardize the definition but to report the results when the term is defined in this manner. The lack of intra- and interobserver assessment for radiographic evaluation may have been a limitation of the present study; however, a previous study16 found excellent intraobserver agreement and good interobserver agreement when evaluating both the fat pad sign and degenerative sign. Previously, grading scales have been used for radiographic evaluation of canine stifle joint disease.16,20,28 These scales are often based on the individual observer's interpretation, rather than on specific descriptors or set limits.16,20,28 In the present study, we chose not to use a grading scale but rather to use the presence or absence of the fat pad sign and degenerative sign for simplicity of clinical application.
Historically, various terms have been used to describe CrCL rupture, including CrCL deficiency and CrCL disease.1,4,6,14 On the basis of a current surgery reference, the term CrCL disease is now used to encompass all disorders affecting the CrCL, which include avulsion fracture of the proximal or distal attachment sites, acute traumatic rupture secondary to excess strain, and pathological rupture from progressive ligamentous failure of unknown cause.24 Avulsion fracture of the CrCL attachment sites is an uncommon injury and occurs primarily in young, skeletally immature dogs.24 In the present study, there were no dogs with CrCL avulsion fractures. Because of unknown factors, dogs with unilateral pathological CrCL rupture should be at high risk for subsequent contralateral CrCL rupture, with the risk for subsequent rupture for dogs with unilateral acute traumatic rupture dependent on the reoccurrence of the initiating extrinsic events that precipitated the initial CrCL rupture; however, distinguishing between an acute traumatic rupture and pathological rupture often presents a clinical challenge because distinction is made on the basis of historical information from the owners and on physical examination, radiographic, and surgical findings. The 2 disorders may actually represent a spectrum of disease, with both extrinsic and intrinsic factors serving a role to varying degrees. Even among Newfoundlands, for which a genetic basis for CrCL rupture has been found, the low inheritance suggests that extrinsic factors have moderate to high association with the development of CrCL rupture.29,30 In the present study, we did not try to separate these 2 reported clinical entities of CrCL rupture because we felt they represent variations of the same condition. Acute traumatic CrCL rupture and pathological rupture were also not distinguished in previous studies.12,13,17,18
Although board-certified surgeons evaluated most of the dogs with subsequent contralateral CrCL rupture, primary care veterinarians evaluated most dogs without subsequent rupture. Telephone follow-up for these dogs relied on subjective data. Another study limitation was the dependence on clients seeking veterinary care for time-to-event follow-up data. This type of population bias is an inherent problem for retrospective clinical studies. Many owners may become aware of the contralateral injury but choose to wait before bringing their dog to the veterinarian because of financial or other reasons. There can also be a lack of follow-up with the initial referring veterinarian for many reasons. Several cases were censored in the early part of this study, particularly for the groups without a contralateral fat pad sign or contralateral degenerative sign. The true long-term status of these dogs was unknown and could have affected the results. Another limitation was the inconsistent description of how cranial tibial instability was assessed. All stifle joints were assessed for cranial tibial instability without sedation or anesthesia, but it was not possible to determine from the medical record the number of stable stifle joints reassessed during sedation or anesthesia. Tibial compression radiography is more sensitive and specific than palpation for identifying cranial tibial instability31 but was not used in the present study.
The aim of this study was to evaluate the contralateral fat pad sign and contralateral degenerative sign as potential risk factors of subsequent contralateral CrCL rupture. We tried to account for potential confounding variables; however, we did not specifically evaluate these variables as potential risk factors. We also did not compare the variables of dogs with bilateral versus unilateral CrCL rupture. In light of the recent focus on deformities of the proximal portion of the tibia as a potential cause of CrCL rupture, we elected to include the TPA and tibial mechanical joint orientation angles as potential confounding variables. Apart from the mechanical caudoproximal tibial angle (mechanical caudoproximal tibial angle = 90° – TPA), variations in the tibial mechanical joint orientation angles have not been evaluated as potential risk factors of CrCL rupture. Despite this, they are a good measure of tibial alignment, and we felt it was reasonable to include them as potential confounding variables.
The contralateral fat pad sign and contralateral degenerative sign were prevalent in dogs with unilateral CrCL rupture and were significant risk factors for subsequent contralateral CrCL rupture. The high prevalence of the contralateral fat pad sign and contralateral degenerative sign and its association with the greatly reduced time to subsequent rupture suggest that many dogs with previously diagnosed unilateral CrCL rupture and a positive contralateral fat pad sign have subclinical bilateral CrCL rupture. These results support the use of bilateral stifle joint radiography for all dogs with CrCL rupture. With such a high prevalence of subsequent contralateral CrCL rupture, the results of this study also support the practice of performing bilateral stifle joint arthroscopy and preemptive surgical stabilization for any dog with a subclinical CrCL rupture in the contralateral stifle joint. Future study involving bilateral stifle joint arthroscopy in a large population of dogs with unilateral CrCL rupture and a positive contralateral fat pad sign is warranted.
ABBREVIATIONS
| CrCL | Cranial cruciate ligament |
| CI | Confidence interval |
| TPA | Tibial plateau angle |
OsiriX, version 3.8.1, Pixmeo, Bernex, Switzerland.
Stata/IC, version 10.1, StataCorp LP, College Station, Tex.
References
1. Witsberger TH, Villamil JA, Schultz LG, et al. Prevalence of and risk factors for hip dysplasia and cranial cruciate ligament deficiency in dogs. J Am Vet Med Assoc 2008; 232: 1818–1824.
2. Hayashi K, Frank JD, Dubinsky C, et al. Histologic changes in ruptured canine cranial cruciate ligament. Vet Surg 2003; 32: 269–277.
3. Morris E, Lipowitz AJ. Comparison of tibial plateau angles in dogs with and without cranial cruciate ligament injuries. J Am Vet Med Assoc 2001; 218: 363–366.
4. Wilke VL, Conzemius MG, Besancon MF, et al. Comparison of tibial plateau angle between clinically normal Greyhounds and Labrador Retrievers with and without rupture of the cranial cruciate ligament. J Am Vet Med Assoc 2002; 221: 1426–1429.
5. Reif U, Probst CW. Comparison of tibial plateau angles in normal and cranial cruciate deficient stifles of Labrador Retrievers. Vet Surg 2003; 32: 385–389.
6. Ragetly CA, Evans R, Mostafa AA, et al. Multivariate analysis of morphometric characteristics to evaluate risk factors for cranial cruciate ligament deficiency in Labrador Retrievers. Vet Surg 2011; 40: 327–333.
7. Paley D. Sagittal plane deformities. In: Herzenberg JE, ed. Principles of deformity correction. Berlin: Springer-Verlag, 2002;155–174.
8. Paley D. Malalignment and malorientation in the frontal plane. In: Herzenberg JE, ed. Principles of deformity correction. Berlin: Springer-Verlag, 2002;19–30.
9. Dismukes DI, Tomlinson JL, Fox DB, et al. Radiographic measurement of the proximal and distal mechanical joint angles in the canine tibia. Vet Surg 2007; 36: 699–704.
10. Dismukes DI, Tomlinson JL, Fox DB, et al. Radiographic measurement of canine tibial angles in the sagittal plane. Vet Surg 2008; 37: 300–305.
11. Fox DB, Tomlinson JL. Principles of angular limb deformity correction. In: Tobias KM, Johnston SA, eds. Veterinary surgery: small animal. St Louis: Saunders Elsevier, 2012;657–668.
12. Cabrera SY, Owen TJ, Mueller MG, et al. Comparison of tibial plateau angles in dogs with unilateral versus bilateral cranial cruciate ligament rupture: 150 cases (2000–2006). J Am Vet Med Assoc 2008; 232: 889–892.
13. Buote N, Fusco J, Radasch R. Age, tibial plateau angle, sex, and weight as risk factors for contralateral rupture of the cranial cruciate ligament in Labradors. Vet Surg 2009; 38: 481–489.
14. Doverspike M, Vasseur PB, Harb MF, et al. Contralateral cranial cruciate ligament rupture: incidence in 114 dogs. J Am Anim Hosp Assoc 1993; 29: 167–170.
15. Moore KW, Read RA. Cranial cruciate ligament rupture in the dog—a retrospective study comparing surgical techniques. Aust Vet J 1995; 72: 281–285.
16. de Bruin T, de Rooster H, Bosmans T, et al. Radiographic assessment of the progression of osteoarthrosis in the contralateral stifle joint of dogs with a ruptured cranial cruciate ligament. Vet Rec 2007; 161: 745–750.
17. Grierson J, Asher L, Grainger K. An investigation into risk factors for bilateral canine cruciate ligament rupture. Vet Comp Orthop Traumatol 2011; 24: 192–196.
18. Muir P, Schwartz Z, Malek S, et al. Contralateral cruciate survival in dogs with unilateral non-contact cranial cruciate ligament rupture. PLoS ONE 2011; 6:e25331.
19. Erne JB, Goring RL, Kennedy FA, et al. Prevalence of lymphoplasmacytic synovitis in dogs with naturally occurring cranial cruciate ligament rupture. J Am Vet Med Assoc 2009; 235: 386–390.
20. Bleedorn JA, Greuel EN, Manley PA, et al. Synovitis in dogs with stable stifle joints and incipient cranial cruciate ligament rupture: a cross-sectional study. Vet Surg 2011; 40: 531–543.
21. Jacobson JA, Girish G, Jiang Y, et al. Radiographic evaluation of arthritis: degenerative joint disease and variations. Radiology 2008; 248: 737–747.
22. Widmer WR, Beckwalter KA, Braunstein EM, et al. Radiographic and magnetic resonance imaging of the stifle joint in experimental osteoarthritis of dogs. Vet Radiol Ultrasound 1994; 35: 371–383.
23. Piermattei D, Flo GL, DeCamp C. The stifle joint. In: Fathman L, ed. Brinker, Piermattei and Flo's handbook of small animal orthopedics and fracture repair. 4th ed. St Louis: Saunders-Elsevier, 2006;582–585.
24. Kowaleski MP, Boudrieau RJ, Pozzi A. Stifle joint. In: Tobias KM, Johnston SA, eds. Veterinary surgery: small animal. St Louis: Saunders Elsevier, 2012;914–920.
25. Laflamme DP. Development and validation of a body condition score system for dogs. Canine Pract 1997; 22: 10–15.
26. McCarthy TC. Synovitis in dogs with stable stifle joints and incipient cranial cruciate ligament rupture (lett). Vet Surg 2012; 41: 540.
27. Hulse D, Beale B, Kerwin S. Second look arthroscopic findings after tibial plateau leveling osteotomy. Vet Surg 2010; 39: 350–354.
28. Innes JF, Costello M, Barr FJ, et al. Radiographic progression of osteoarthritis of the canine stifle joint: a prospective study. Vet Radiol Ultrasound 2004; 45: 143–148.
29. Wilke VL, Zhang S, Evans RB, et al. Identification of chromosomal regions associated with cranial cruciate ligament rupture in a population of Newfoundlands. Am J Vet Res 2009; 70: 1013–1017.
30. Wilke VL, Conzemius MG, Kinghorn BP, et al. Inheritance of rupture of the cranial cruciate ligament in Newfoundlands. J Am Vet Med Assoc 2006; 228: 61–64.
31. de Rooster H, Van Ryssen B, van Bree H. Diagnosis of cranial cruciate ligament injury in dogs by tibial compression radiography. Vet Rec 1998; 142: 366–368.
